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Human Diseases > 24.1 Neurology for dentistry > Flashcards

24.1 Neurology for dentistry Flashcards

1
Q

CN I.

A
  • Olfactory
  • Sensory
  • Sense of smell
  • Ask about change in smell
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2
Q

CN II.

A
  • Optic
  • Sensory
  • Vision
  • Visual acuity via Snellen chart, visual fields
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3
Q

CN III.

A
  • Oculomotor
  • Motor
  • Extrinsic and extrinsic eye movements, levator palpebrae superioris
  • Eye movements, accomodation reflex, pupil reflex, eyelid opening
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4
Q

CN IV.

A
  • Trochlear
  • Motor
  • Innervates superior oblique muscle of the eye
  • Eye movements
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4
Q

CN V.

A
  • Trigeminal
  • Both (motor and sensory)
  • Sensation to the face, motor to muscles of mastication, mylohyoid, anterior belly of digastric, tensor tympani and tensor veli palatini
  • Light touch, jaw movement, clenching of muscles
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5
Q

CN VI.

A
  • Abducens
  • Motor
  • Lateral rectus muscle
  • Eye movements
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6
Q

CN VII.

A
  • Facial
  • Both and autonomic (parasympathetic)
  • M: Muscles of facial expression, posterior belly of digastric, stylohyoid and strapedius
  • S: taste to anterior 2/3rds of the tongue
  • Parasymp: lacrimal glands and salivary glands
  • Test the facial muscles (branches TZBMC)
  • Reduced salivation and loss of taste
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7
Q

CN VIII.

A
  • Vestibulocochlear
  • Sensory
  • Hearing
  • Weber and Rinne test
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8
Q

CN IX.

A
  • Glossopharnygeal
  • Both and autonomic
  • M: stylopharyngeus muscle
  • S: taste to posterior third of tongue and palate
  • Autonomic: parotid gland
  • Test gag reflex
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9
Q

CN X.

A
  • Vagus nerve
  • Both and autonomic
  • M: pharyngeal constrictors, cricothyroid muscle, palatoglossus, palatopharyngeaus, muscles of larynx
  • S: visceral sensation to heart and abdomen viscera, taste to epiglottis and root of tongue
  • Motor parasympathetic: innervates the smooth muscle of the trachea, bronchi and gastro-intestinal tract and regulates heart rhythm
  • Pt says ‘ah’ observe the uvula
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10
Q

CN XI.

A
  • Accessory
  • Motor
  • Sternocleidomastoid and trapezius
  • Askpt to shrug shooulders and turn head against resistance
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11
Q

CN XII.

A
  • Hypoglossal
  • Motor
  • Muscles of tongue
  • Stick tongue out
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12
Q

What is mydriasis?

A

Dilation of the pupil

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13
Q

What is ptosis?

A

Drooped eyelid

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14
Q

What cranial nerve is damaged?

A
  • Cranial nerve III defect (oculomotor)
  • Eyeball is down and out, pupil is dilated as constrictor muscle has lost its tone, ptosis, mydriasis
  • Oculomotor nerve palsy
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15
Q

What cranial nerve is damaged?

A
  • CN VI (abducens) nerve palsy
  • Lateral rectus not functioning correctly
16
Q

What cranial nerve is damaged?

A
  • Hypoglossal (VII), left
  • Muscles on left side are weaker and tongue curves towards the damaged side as it is a lower motor neuron defect
17
Q

Compare a lower motor neuron defect vs upper motor neuron defect.

A
  • Lower motor neuron defect = nerve itself affected
  • Upper motor neuron defect = higher up brain/neuron issues

Example if hypoglossal nerve is damaged:
- Lower defect – tongue curves towards damaged side, in this case it is a left lower motor neuron defect
- Upper defect – tongue would curve away from damaged side

18
Q

What cranial nerve is damaged?

A
  • Right facial nerve palsy
  • Lower motor neuron defect
  • If it was an upper motor neuron defect you would still get some eyebrow furrowing/eyebrow sparing
19
Q

What cranial nerve is damaged?

A
  • Right accessory nerve palsy (XI)
  • Most commonly seen in pts who have undergone neck dissection
  • Accessory nerve is very narrow and easily damaged
20
Q

What is a cerebrovascular accident?

A

A stroke

21
Q

What are the 3 types of stroke?

A
  • Ischaemic: caused by a thrombus or embolus in the brain, blocks the brain and causes an infarction
  • Haemorrhagic (approx. 15%): caused by a bleed, causes infarction
  • Transient ischaemic attack (TIA): not technically a stroke, temporary reduced blood supply to the brain but no infarction, known as a mini stroke, may go on to have a stroke
22
Q

What are the risk factors for a stroke?

A
  • Cardiovascular disease such as angina, MI, peripheral cardiovascular disease
  • Previous stroke or TIA
  • Atrial fibrillation, pts often on Rivaroxaban as prevention
  • Carotid artery disease- atherosclerotic, plaque breaks off and spreads to carotid artery
  • Hypertension
  • Diabetes
  • Smoking
  • Vasculitis
  • Thrombophilia
  • Combined contraceptive pill
23
Q

How is a stroke recognised?

A

FAST
- Facial weakness
- Arm weakness
- Slurred speech
- Time

24
Q

What should you do if you suspect a stroke in dental practice?

A
  • Call 999
  • Do not give aspirin
  • Give supplemental oxygen if saturation is below 92%, 15 litres per min
  • Continue monitoring patient via ABCDE approach
  • Get someone to take notes and note timings of onset of symptoms or any change of symptoms
  • Handover to ambulance crew using SBAR format
  • SBAR: situation, background, assessment, recommendation
25
Q

How are strokes treated in hospital?

A
  • CT to exclude haemorrhage
  • Give 300mg if it is not a haemorrhagic stroke, continue 300mg aspirin daily for 2 weeks
  • Thrombolysis: e.g. alteplase, a tissue plasminogen activator, breaks down clots and reverses effects of stroke, helps to save brain tissue
26
Q

What is the secondary prevention of stroke following an ischaemic stroke or TIA?

A
  • Clopidogrel 75mg daily (antiplatelet)
  • Atorvastatin 80mg daily
27
Q

What is motor neuron disease?

A

An umbrella term to describe a vairety of types of diseases affecting the motor neurons only (not sensory), a progressive and ultimately fatally condition.
Most common MND is ALS: amyotrophic lateral sclerosis

28
Q

What is the presentation of MND?

A
  • Insidious progressive weakness of all muscles
  • Affects speech
  • Usually first noticed in upper limbs
  • Clumsiness, tripping over
  • Slurred speech
  • Dysphagia
  • Lower motor neuron disease: muscle wasting, reduced tone and fasciculations in muscles
29
Q

What is the management for NMD?

A
  • No effective treatment
  • Medication can ease symptoms
  • Riluzole can slow progression of ALS and extend survival by a few months
  • Pts usually die of respiratory failure or pneumonia
30
Q

What is myasthenia gravis?

A

An autoimmue condition caused by antibodies attacking components of the post synaptic membrane.
More common in women under 40 and men over 60.
Linked with thymoma- tumour of the thymus gland.

31
Q

What antibodies are present in pts with myasthenia gravis?

A
  • 85% have acetyl choline receptor antibodies
  • 15% have antibodies to muscle-specific kinase (MuSK) or low density lipoprotein receptor related protein 4 (LRP4) - both needed for creation of acetyl choline receptors

Receptors are blocked meaning AP can’t be generated.

32
Q

What are the symptoms of myasthenia gravis?

A

The symptoms most affect the proximal muscles and small muscles of the head and neck. Leading to:
- Extraocular muscle weakness causing double vision (diplopia)
- Eyelid weakness causing drooping of the eyelids (ptosis)
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in the jaw when chewing
- Slurred speech
- Progressive weakness with repetitive movements

33
Q

How is myasthenia gravis treated?

A
  • Reverisble acetylcholinesterase inhibtitors e.g. pyridostigmine or neostigmine
  • Immunosuppression e.g. prednisolone or azathioprine
  • Thymectomy can improve symptoms even in patients without a thymoma
  • Biologics
34
Q

Describe biologics in relation to the treatment of myasthenia gravis.

A
  • Monoclonal antibodies
  • End in ‘mab’
  • Rituximab targets B cells and reduces the production of antibodies
  • Eculizumab targets complement protein C5, prevents complement activation and destruction of acetylcholine receptors
  • Biologics have immunosuppresive actions
35
Q

What are the dental implications of myasthenia gravis?

A

Human Diseases (47 decks)

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